摘要
目的探讨腺苷预处理对人未成熟心肌缺血再灌注损伤的保护作用机制。方法将42例5周岁以下行室间隔缺损修补术的患儿采用数字表法随机分成腺苷组(A组)和对照组(B组),每组21例。腺苷组在体外转流前经颈内静脉插管直接向上腔静脉滴注腺苷进行预处理,对照组亦在体外转流前经相同路径滴入等量的0.9%氯化钠溶液。然后在体外循环前(T1)、体外循环结束即刻(T2)、主动脉开放1h(T3)、主动脉开放3h(T4)、主动脉开放24h(T5)分别取血检测丙二醛(malondialdehyde,MDA)、TNF-α、IL-10的含量及红细胞压积(HCT),并分别在主动脉阻断前和主动脉开放15min取右心房相同部位少量心肌组织(约2mm3),电镜观察其超微结构的改变情况。结果两组患儿MDA、TNF-α、IL-10浓度均于体外循环开始后显著升高(P<0.01),MDA及IL-10浓度在T3时点达最高,TNF-α浓度在T4时点达最高,此后开始下降。腺苷组T3、T4时点MDA浓度较T1时点显著增高(P<0.01),对照组T3、T4、T5时点MDA浓度较T1时点显著增高(P<0.01),而且腺苷组MDA浓度在T2、T3、T4、T5各时点均显著低于对照组(P<0.01);两组患儿T2、T3、T4、T5各时点的TNF-α及IL-10浓度均显著高于T1时点(P<0.01),而且腺苷组T2、T3、T4、T5各时点的TNF-α浓度均显著低于对照组(P<0.01),T3、T4、T5时点IL-10浓度均显著高于对照组(P<0.01)。此外,电镜下观察可见,腺苷组心肌线粒体轻度肿胀,少许空泡变性,肌浆网水肿,肌膜下轻微水肿,肌丝间隙稍增大;对照组心肌线粒体肿胀及空泡样变性明显,肌丝排列紊乱,部分肌丝溶解断裂。结论减轻炎症反应可能是腺苷预处理对人未成熟心肌缺血再灌注损伤的保护作用机制之一。
Objective To explore the mechanism of adenosine preconditioning in protection of immature human myocardium under ischemic reperfusion injury. Methods Forty-two children undergoing remedy operation for ventricular septal defect （VSD） under cardiopulmonary bypass （CPB） were preoperatively randomized into adenosine group （group A, n=21） and control group （group B, n=21）. In group A adenosine was infused into superior vena cava via internal jugular vein before CPB; in group B, the same amount of NS was infused instead of adenosine. The blood malondialdehyde （MDA）, TNF-α, IL-10 and HCTwere measured before CPB （T1）,immediately after CPB （T2）, 1 h （T3）, 3 h （T4） and 24 h（T5）after aortic unclamping. Right atrium myocardial biopsy was performed before aortic clamping （T6） and 15 min after aortic unclamping （T7） for electron microscopic examination. Results There were no significant differences in plasma levels of MDA, TNF-α and IL-10 between two groups before CPB （P〉0.05）. The plasma levels of MDA elevated after CPB （P〈0.01） and reached the peak value at T3, then declined in two groups. At T2, T3, T4 and T5, the plasma levels of MDA in group A were significantly lower than those in group B. The plasma levels of TNF- α in two groups elevated gradually during CPB and reached the peak value at T4, then began to decline. The value of TNF-α during CPB were higher than that before CPB （P〈0.01）. The plasma levels of TNF-α in group A were significantly lower than those in group B after CPB （P〈0.01）. The plasma levels of IL-10 began to elevate gradually during CPB and reached the peak value at the end of CPB （T3） in two groups. The plasma levels of IL-10 in group A were significantly higher than those in group B after time point T3 （P〈0.01）. The change of myocardial ultrastructure after CPB： There were mild mitochondria swelling, little vacuolation, mild subsarcolemmal swelling, reduced atrium granules and increased myofilament interspace in g
出处
《浙江医学》
CAS
2008年第7期685-688,共4页
Zhejiang Medical Journal
关键词
腺苷
预处理
未成熟心肌
缺血再灌注损伤
Adenosine Preconditioning Premature myocardium Ischemic reperfusion injury
